Motor control in mice gained increasing interest, since transgenic and mutant mice strains have been generated with different motor disorders resembling symptoms of human diseases. But since results from cats can not directly be transferred to mice investigations of mutated murine motor circuitries require further results from wild-type mice. Therefore, we now investigated the lumbar motor reflex pattern in mice in comparison to that in cats with intracellular motoneuronal recording and monosynaptic reflex testing in fully anaesthetized mice (initially pentobarbital sodium 70 mg/kg i.p., continuance with methohexital sodium 60–70 mg/kg/h i.v.). Some results in mice were similar to those in cats: (1) monosynaptic EPSPs had a threshold slightly above 1T (T = threshold for the lowest threshold fibres) and were maximal with around 2T; (2) group II EPSPs had a threshold around 1.5T and were maximal at 5-8T ; (3) group III EPSPs had a threshold above 7- 10T; (4) latencies to the group I incoming volley were below 1ms for monosynaptic group I EPSPs, around 3ms for polysynaptic group II EPSPs and above 4ms for group III EPSPs. However, in contrast to reflex actions in cats, the sural nerve evoked a monosynaptic reflex in mice and group II and III EPSPs clearly dominated in tibial (including flexor digitorum longus and gastrocnemius–soleus) motoneurones, moreover monosynaptic reflexes of the extensor gastrocnemius-soleus were facilitated by conditioning stimulation of the peroneal, sural and tibial nerves, i.e. by different flexor reflex afferents. This facilitation persisted after high lumbar spinalization. Possibly, the observed difference between mice and cats is due to differences in the performance of propulsion during locomotion.